Eye Movements Take Edge off Traumatic Memories

Summary: Researchers report EMDR, a widely used but controversial psychotherapy technique, can help suppress fear related amygdala activity during the recall of traumatic memories.

Source: SfN.

Two human experiments published in Journal of Neuroscience demonstrate that a widely used yet controversial psychotherapy technique suppresses fear-related amygdala activity during recall of a traumatic memory.

WDespite being a common and evidence-based therapy, Eye Movement Desensitization and Reprocessing (EMDR) — discovered serendipitously in 1987 by a psychologist while walking in the woods — it is unclear whether the eye movements in this treatment provide any additional benefits to patients struggling with fear-related disorders that are not readily achieved through traditional exposure therapy.

The promise of EMDR is its potential to recode the emotional content of the traumatic memory itself.

Investigating the neurobiological mechanisms underlying EMDR in healthy men and women, Lycia de Voogd and colleagues found that both side-to-side eye movement and a working memory task independently deactivated the amygdala — a brain region critical for fear learning.

Two human experiments published in JNeurosci demonstrate that a widely used yet controversial psychotherapy technique suppresses fear-related amygdala activity during recall of a traumatic memory. NeuroscienceNews.com image is credited to de Voogd et al., JNeurosci (2018).

The researchers show in a second experiment that this deactivation enhanced extinction learning — a cognitive behavioral technique that reduces the association between a stimulus and a fear response.

The reduced amygdala activity is thought to be a consequence of less available resources since they are dedicated to making eye movements.

About this neuroscience research article

Funding: This work was supported by EMDR Research Foundation, European Research Council.

Improving extinction learning is essential to optimize psychotherapy for persistent fear-related disorders. In two independent studies (both n=24), we found that goal-directed eye movements activate a dorsal fronto-parietal network and transiently deactivate the amygdala ([graphic1]=.17). Connectivity analyses revealed that this down-regulation potentially engages a ventromedial prefrontal pathway known to be involved in cognitive regulation of emotion. Critically, when eye movements followed memory reactivation during extinction learning, it reduced spontaneous fear recovery 24 hours later ([graphic2]=.21). Stronger amygdala deactivation furthermore predicted a stronger reduction in subsequent fear recovery after reinstatement (r=.39). In conclusion, we show that extinction learning can be improved with a non-invasive eye-movement intervention that triggers a transient suppression of the amygdala. Our finding that another task which taxes working memory leads to a similar amygdala suppression furthermore indicates that this effect is likely not specific to eye movements, which is in line with a large body of behavioral studies. This study contributes to the understanding of a widely used treatment for traumatic symptoms by providing a parsimonious account for how working memory tasks and goal-directed eye movements can enhance extinction-based psychotherapy, namely through neural circuits (e.g., amygdala deactivation) similar to those that support cognitive control of emotion.

Significant statement

Fear-related disorders represent a significant burden on individual sufferers and society. There is a high need to optimize treatment, in particular via non-invasive means. One potentially effective intervention is execution of eye movements following trauma recall. However, a neurobiological understanding of how eye movements reduce traumatic symptoms is lacking. We demonstrate that goal-directed eye-movements, like working memory tasks, deactivate the amygdala, the core neural substrate of fear learning. Effective connectivity analyses revealed amygdala deactivation potentially engaged dorsolateral and ventromedial prefrontal pathways. When applied during safety learning, this deactivation predicts a reduction in later fear recovery. These findings provide a parsimonious and mechanistic account of how behavioral manipulations taxing working memory and suppressing amygdala activity can alter retention of emotional memories.

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2 Responses

I am licensed psychologist doing trauma therapy for over thirty years. I have found that a variety of techniques that deactivate the amygdala while bringing up a traumatic memory helps to counter condition the traumatic memory before the memory becomes reconsolidated. These therapies have a lasting effect for approximately ninety percent of the clients that I have treated. EMDR is one of these effective techniques. Self applied acupressure and other energy psychology techniques also are effective clinically, as are hypnotherapy techniques. Dr. Wolpe’s research with progressive relaxation and systematic desensitization also yield similar results and provide a theoretical basis for counter conditioning the fight/flight/freeze response that the amygdala has encoded. In this regard, this nueroscience research supports what I have found to be true clinically and what has been researched by the different treatment regimens. Clinically, it is important to adjust the treatment to the client and realize that different therapies are useful for different clients under different situations.

Of course EMDR does that – it also activates the parasympathetic system. Does every one with a traumatic event need the parasympathetic system activated? No, maybe a small percentage but the remainder then develop an on-going need to repeat EMDR to feel better. Do a certain number of EMDR sessions reset the brain for allostatic load in an on-going manner? For the majority of users it seems unlikely.